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@ARTICLE{Park:130298,
      author       = {J.-S. Park and I.-K. Kim and S. Han and I. Park and C. Kim
                      and J. Bae and S. J. Oh and S. Lee and J. H. Kim and D.-C.
                      Woo and Y. He and H. Augustin$^*$ and I. Kim and D. Lee and
                      G. Y. Koh},
      title        = {{N}ormalization of {T}umor {V}essels by {T}ie2 {A}ctivation
                      and {A}ng2 {I}nhibition {E}nhances {D}rug {D}elivery and
                      {P}roduces a {F}avorable {T}umor {M}icroenvironment.},
      journal      = {Cancer cell},
      volume       = {30},
      number       = {6},
      issn         = {1535-6108},
      address      = {Cambridge, Mass.},
      publisher    = {Cell Press},
      reportid     = {DKFZ-2017-05377},
      pages        = {953 - 967},
      year         = {2016},
      abstract     = {A destabilized tumor vasculature leads to limited drug
                      delivery, hypoxia, detrimental tumor microenvironment, and
                      even metastasis. We performed a side-by-side comparison of
                      ABTAA (Ang2-Binding and Tie2-Activating Antibody) and ABA
                      (Ang2-Blocking Antibody) in mice with orthotopically
                      implanted glioma, with subcutaneously implanted Lewis lung
                      carcinoma, and with spontaneous mammary cancer. We found
                      that Tie2 activation induced tumor vascular normalization,
                      leading to enhanced blood perfusion and chemotherapeutic
                      drug delivery, markedly lessened lactate acidosis, and
                      reduced tumor growth and metastasis. Moreover, ABTAA
                      favorably altered the immune cell profile within tumors.
                      Together, our findings establish that simultaneous Tie2
                      activation and Ang2 inhibition form a powerful therapeutic
                      strategy to elicit a favorable tumor microenvironment and
                      enhanced delivery of a chemotherapeutic agent into tumors.},
      keywords     = {Antibodies (NLM Chemicals) / Antineoplastic Agents (NLM
                      Chemicals) / Dacarbazine (NLM Chemicals) / Receptor, TIE-2
                      (NLM Chemicals) / Tek protein, mouse (NLM Chemicals) / Ang2
                      protein, mouse (NLM Chemicals) / Ribonuclease, Pancreatic
                      (NLM Chemicals) / temozolomide (NLM Chemicals)},
      cin          = {A190},
      ddc          = {610},
      cid          = {I:(DE-He78)A190-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:27960088},
      doi          = {10.1016/j.ccell.2016.10.018},
      url          = {https://inrepo02.dkfz.de/record/130298},
}